Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 11 instances (6%) of 183 consecutive hepatic angiograms done for subsequently proven pathologic hepatic processes, either the diagnosis was incorrect (4 patients) or a satisfactory differential diagnosis was not established (7 patients), despite obvious angiographic abnormalities. Incorrect diagnoses were made in patients with suppurative hapatocarcinoma and liver cyst, macronodular regenerative cirrhosis, and multiple intrahepatic abscesses. Satisfactory differential diagnoses could not be established in patients with enlarged intrahepatic ducts, acute viral hepatitis, recurrent cirrhosis and acute liver necrosis. On analysis, means for minimizing diagnostic failure include the use of enhancement techniques such as infusion angiography and pharmacoangiography and an unbiased, detailed analysis of the angiographic findings. Changes secondary to the pathologic process and the coexistence of multiple processes, however, can occasionally prevent an accurate diagnosis.
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PMID:Limitations of angiographic differential diagnosis in major hepatic processes. 19 85

The morphologic type of cirrhosis that is followed most frequently by hepatocellular carcinoma is posthepatitic cirrhosis. Furthermore, HB AG is detected in a high rate among cases with hepatocellular carcinoma suggesting the intimate causal relationship between hepatitis b virus and hepatocellular carcinoma. It has been considered that hepatocellular carcinoma might develop during destruction and regeneration of fully developed liver cirrhosis. However, hepatocellular carcinoma is combined with not only liver cirrhosis but also with mild liver fibrosis. An attempt was made to determine HBs Ag in the liver tissue of liver fibrosis with hepatocellular carcinoma. HBs Ag was found in non-cancerous liver tissue of 40 percent of those cases. Therefore, it may be concluded that, at least some of those fibrosis is caused by chronic viral hepatitis and hepatocellular carcinoma may develop not only on posthepatitic cirrhosis but also on chronic persistent hepatitis. This evidence also suggests the carcinogenicity of hepatitis B virus.
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PMID:Hepatocellular carcinoma and chronic persistent hepatitis. 20 57

The chief causes of liver disease in Ethiopia are reviewed, considering hospital data on admissions for hepatitis, cirrhosis, ascites and hepatoma. Liver diseases account for 11.4% of all medical admissions in 3 medical wards in Addis Ababa. The causes are viral hepatitis, post- hepatic and post necrotic and mixed cirrhosis and hepatocellular carcinoma. Alcoholic cirrhosis is rare. Viral hepatitis with shivering, rigor and fever and elevated direct bilirubin levels are common in Ethiopians, especially in child-bearing women. The hepatitis B surface antigen (HBsAg) is often associated with hepatitis. The disease may be transmitted by several species of mosquitoes, placental transmission, or feces, urine, saliva or semen. Blood products are not screened for hepatitis B. Cirrhosis is common, and causes significant mortality, usually from esophageal varices and hepatic coma. Chronic active hepatitis patients may live for a time, especially if they are near a hospital and are treated with steroids. In Ethiopia presenting symptoms for hepatoma are anorexia, weight loss, persistent, burning, right upper quadrant pain, and a hard, nodular, tender RUQ mass. Over 5% of malignancies seen are primary hepatocellular carcinomas. 50% have HBsAG, compared to 3.8% of controls. 65% have alpha-fetoglobulins. It is suggested that some viral hepatitis cases progress to cirrhosis, of which some go on to hepatocellular carcinoma. Herbal medicines, aflatoxins and other toxins may also contribute to liver disease.
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PMID:Current views on liver diseases in Ethiopia. 20 62

An electroneurographic study performed on the peripheral nerves of 25 patients with severe cirrhosis following viral hepatitis showed slight slowing (P greater than 0.05) of motor conduction velocity (CV) and significant diminution (P less than 0.001) of sensory CV and mixed sensorimotor-evoked potentials, associated with a significant decrease in the amplitude of sensory evoked potentials. The slowing was about equal in the distal (digital) and in the proximal segments of the same nerve. A mixed axonal degeneration and segmental demyelination is presumed to explain these findings. The CV measurements proved helpful for an early diagnosis of hepatic polyneuropathy showing subjective symptoms in the subclinical stage.
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PMID:Electroneurographic evidence of polyneuropathy in chronic liver disease. 20 28

Serum albumin and total globulin were determined in 22 healthy people, 29 patients with acute viral hepatitis, 27 patients with cirrhosis and 27 patients with primary hepatocellular carcinoma to see if they might be of discriminating value. The mean serum albumin values were found to be highest in the healthy subjects followed by acute viral hepatitis, primary hepatocellular carcinoma and cirrhosis, in that order. The mean serum total globulin values on the other hand, were found to be lowest in the healthy subjects followed by acute viral hepatitis, primary hepatocellular carcinoma and cirrhosis, in that order. Both the mean albumin and mean total globulin of each group of subjects were significantly different from the respective means of the other three groups. A probable explanation for the higher serum albumin and lower globulin levels found in primary hepatocellular carcinoma, as compared to cirrhosis, is that hepatocellular carcinoma occurs in reasonably well-compensated cases of cirrhosis.
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PMID:Serum albumin and total globulin levels in common liver diseases in Accra (Ghana). 20 91

Serum angiotensin I converting enzyme, identical with kininase II, was measured fluorometrically in patients with acute viral hepatitis (n=18), liver cirrhosis without (n=44) and with (n=19) ascites. In all groups of patients the enzyme was significantly elevated as compared to 44 healthy controls (p less than 0.001). No correlation could be found between angiotensin I converting enzyme activity and liver function tests (serum glutamic oxalacetic transaminase, serum glutamic pyruvic transaminase, total protein, albumin, bilirubin) or other parameters (serum potassium, serum sodium). High serum converting enzyme activity in chronic liver diseases might originate primarily from an altered pulmonary circulation and indicates higher conversion rate of angiotensin I by passage through the lungs as well as increased bradykinin degradation. The reason for the enzyme liberation in acute viral hepatitis is as yet uncertain.
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PMID:Changes of serum angiotensin I converting enzyme in patients with viral hepatitis and liver cirrhosis. 22 16

The disposition of phenobarbital (PB) was studied in normal individuals and in patients with cirrhosis or acute viral hepatitis to determine 1) if there is significant impairment of PB metabolism in hepatic disease and 2) to what extent such abnormal disposition of the drug affects its disappearance from blood. The diagnosis of liver disease was based on characteristic clinical findings, biochemical liver "function" tests and liver biopsy when necessary. All individuals had normal renal function and were free of other drug and alcohol intake for at least 3 weeks. With radiotracer methodology, PB and its principal metabolites, p-hydroxyphenobarbital (PBOH) and conjugated PBOH (PBOC), were monitored in blood and urine for 5 days after a single dose of 14-C-PBadministered intraduodenally. PB blood half-life (T1/2) in the control group was 86 plus or minus 3 hours (S.E.). In cirrhotics the T1/2 was prolonged to 130 plus or minus 15 hours (P less than .001) and this was accompanied by a 50% reduction in urinary PBOC excretion (P less than .05). Urinary excretion of PB and PBOH was unaltered by cirrhosis. In patients with acute viral hepatitis, PB T1/2 was not significantly prolonged and urinary excretion of PB and its metabolites was in the normal range (P greater than .05). No PBOH and only traces of PBOC were detected in the blood of either control individuals or patients with liver disease. Urinary excretion of unchanged PB was an important elimination pathway of the drug in all groups. As a result of this, PB T1/2 in cirrhosis was only moderately prolonged.
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PMID:The effect of liver disease in man on the disposition of phenobarbital. 23 36

Grey-scale ultrasound tomography was used to examine the liver and biliary tree of 100 consecutive unselected jaundiced patients in a prospective study. It was successful in differentiating between hepato-cellular and obstructive jaundice in 94%. It precisely localised the site of obstruction in 75% of those patients with enlargement of the head of the pancreas from either carcinoma or gall-stones impacted in the Ampulla of Vater. This figure was reduced to 60% when all cases of obstruction were considered. Cirrhosis and chronic active hepatitis were found to be associated with an abnormal pattern of echoes within the liver. These echoes were stronger and more numerous than normal. This association was not apparent with drug-induced cholestasis or acute viral hepatitis. Grey-scale ultrasound tomography is quick, safe and completely non-invasive. It should be the initial investigation of choice in the differential diagnosis of jaundice. When precise localisation of an obstruction is not possible after a repeat attempt, then percutaneous transhepatic cholangiography should be considered.
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PMID:Ultrasound tomography of the liver: Non-invasive method of choice for the differential diagnosis of jaundice. 28 82

Elevated circulating CEA levels occur in patients with benign gastrointestinal and hepatic disorders. These are usually less than 10 ng/ml. Of clinical importance is the influence of liver disease on the interpretation of CEA. At least 50% of patients with severe benign hepatic disease have elevated CEA levels, most often active alcoholic cirrhosis, and also chronic active and viral hepatitis, and cryptogenic and biliary cirrhosis. Patients with benign extrahepatic biliary obstruction may have increased plasma CEA, the highest in patients with co-existent cholangitis and especially liver abscess. The liver appears to be essential for the metabolism and/or excretion of CEA. Hence, liver work-up is needed to assess any patient with an elevated CEA. A damaged liver may further augment elevated CEA levels due to cancer. The increased circulating CEA observed in some patients with active ulcerative colitis tends to correlate with severity and extent of disease and usually returns to normal with remission. CEA levels also may be mildly elevated in patients with pancreatitis and in adults with colonic polyps. Smoking may contribute to the increased CEA levels seen in patients with alcoholic liver disease and pancreatitis. Therefore, in interpreting mildy elevated circulating CEA levels in patients with GI tract diseases, one must consider benign as well as malignant etiologies.
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PMID:Carcinoembryonic antigen (CEA) levels in benign gastrointestinal disease states. 36 Dec

Thirty patients were studied at the Hacettepe University Medical Center. Ten patients had hepatic cirrhosis, 20 patients had viral hepatitis. HB-Ag in the serum was positive in all patients by the counterimmunoelectrophoresis method. One and a half milliliters of sweat was collected from each patient, dried and dissolved in 0.2 ml. of buffer solution. HB-Ag was positive in all patients by radioimmunoassay method. This study indicates that direct contact is one of the most important factors in the epidemiology of the disease and this may even be more important in asymptomatic carriers.
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PMID:HB-Ag in sweat. 41


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